Introduction
Parkinson’s disease (PD) is associated with deficits in dopaminergic pathways in the brain, most notably those arising from the substantia nigra, though many other areas are involved. PD is characterised by tremor, rigidity, slowness of movement (bradykinesia) and postural imbalance. Potential non-motor symptoms include cognitive impairment, depression, fatigue, apathy, loss of smell and taste, and other sensory disturbances.1
The Unified Parkinson’s Disease Rating Scale (MDS-UPDRS) is the tool most widely used to measure disease status in PD. However, the MDS-UPDRS is problematic in that it is subjective, shows day-to-day fluctuation and inter-observer variability, and does not provide a clinically useful estimate of disease prognosis.2 PD progression rates are very variable across patients,3 and there is therefore an urgent need to identify sensitive, reliable and objective markers to increase diagnostic specificity, determine the current stage of disease, and provide prognostic information.4 One potential marker is measurement of postural control, which shows some promise in identifying and tracking disease progression in early PD.5
A cardinal feature of all forms of Parkinsonism is impairment of posture and balance. Clinically, this manifests as abnormalities of gait and righting reflexes, though abnormalities can be subtle in the early stages.6 7 Postural adjustments made while standing still are easily measured, yielding a sophisticated set of measures of postural sway.8 9 Assessment of postural sway may therefore have a possible role in tracking disease progression and, perhaps, in informing diagnosis and providing prognostic information about patients with PD, either on its own or in combination with other measures.
Postural sway is defined as the movement of the body’s centre of mass (CoM) in the horizontal plane while standing.10 This can be measured by standing subjects on a force plate and detecting movement of the centre of pressure (CoP) in real time. Sway can be evaluated either while subjects are standing still or while they are moving.11 There is evidence that concurrent performance of cognitive tasks affects the pattern of sway in PD,12 even in the prodromal stages of the disease. A study of patients with idiopathic rapid eye movement (REM) sleep behaviour disorder (many of whom went on to develop PD) showed that sway patterns during cognitively challenging conditions could distinguish patients from controls.13 This is consistent with the notion that patients with impaired postural control invoke more conscious, cognitive mechanisms to compensate for their underlying deficit.14
Postural control is a complex neurological process requiring integration of visual, proprioceptive, and vestibular information to ensure that the CoM stays within the base of support.15 Deviation of the centre of mass is detected by proprioceptive and kinaesthetic systems which lead to compensatory motor mechanisms that prevent falling and generate anticipatory mechanisms to prepare the body for upcoming changes in the CoM and/or base of support. These compensatory motor mechanisms require constant updating of motor programmes and corresponding muscle activity over short periods of time. Neurological or musculoskeletal disorders may interfere with rapid updating of these programmes and can therefore result in falls or a highly unstable stance. Impairment in proprioception and kinaesthesia may also prevent detection of small postural fluctuations, leading to a delayed or incorrect motor response.
Postural instability in PD is likely to arise from a combination of disordered proprioception and impaired motor control.16 There is substantial evidence that patients with PD have abnormal proprioception under both passive and active conditions.17 18 The abnormal proprioception exacerbates postural instability,19 but patients appear to be able to compensate by using visual information.20
In addition, patients with PD are often unable to generate appropriately-sized long-latency postural reflexes in response to postural perturbation, consistently underestimating the appropriate muscular response.21 This leads to insufficient postural correction in response to a destabilising stimulus and so increases the risk of falling. In order to compensate for both sensory and motor impairment, patients may employ more cognitive strategies to maintain stable posture. Progressive failure of these strategies as the disease deteriorates would, in turn, result in worsening of postural control. In support of this hypothesis, previous studies have found that cognitive function and mood (anxiety and depression) were correlated with measures of gait and balance in PD.22 23
Another consideration is that the increased muscular rigidity which occurs in PD could reduce spontaneous sway while, on the other hand, dopaminergic therapy might increase sway by reducing rigidity.24 The effects of dopaminergic medication on postural sway are therefore potentially complex.25
This study aimed to investigate the combined use of postural sway, cognition and quality of life to assess disease severity in PD with the ultimate aim of developing a valid, reliable, quantifiable and objective measure of disease status. The tests involved were selected to be robust and time-efficient so that they would translate easily into a clinical setting, thereby having the potential to assist clinicians with diagnosis, measurement of response to treatment, and determination of prognosis. We hypothesised that patients would exhibit increased postural sway in comparison to controls, and that this increase in sway might also be related to cognitive functioning in patients.
